References

Maron BJ, Towbin JA, Thiene G Contemporary definitions and classification of the cardiomyopathies: an American Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation. 2006; 113:1807-1816 https://doi.org/10.1161/CIRCULATIONAHA.106.174287
Cardiomyopathy UK. What is cardiomyopathy. 2018. http://www.cardiomyopathy.org/about-cardiomyopathy (accessed October 2022)
Wexler RK, Elton T, Pleister A, Feldman D. Cardiomyopathy: an overview. Am Fam Physician. 2009; 79:778-784
Cardiomyopathy UK. Dilated cardiomyopathy. http://www.cardiomyopathy.org/dilated-cardiomyopathy (accessed October 2022)
Cardiomyopathy UK. Hypertrophic cardiomyopathy. http://www.cardiomyopathy.org/about-cardiomyopathy/types-cardiomyopathy/hypertrophic-cardiomyopathy (accessed October 2022)
Cardiomyopathy UK. Restrictive cardiomyopathy. http://www.cardiomyopathy.org/about-cardiomyopathy/types-cardiomyopathy/restrictive-cardiomyopathy (accessed October 2022)
Prasad A. What is Takotsubo (stress) cardiomyopathy?. Eur Cardiol. 2015; 10:6-8 10.15420/ecr.2015.10.01.6
Sharkey SW, Windenburg DC, Lesser JR Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol. 2010; 55:333-341 https://doi.org/10.1016/j.jacc.2009.08.057
Chronic heart failure. National clinical guideline for diagnosis and management in primary and secondary care.Salisbury: Sarum Colourview Group; 2003
Elliott PM, Anastasakis A, Borger MA 2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy: the Task Force for the Diagnosis and Management of Hypertrophic Cardiomyopathy of the European Society of Cardiology (ESC). Eur Heart J. 2014; 35:2733-2779 https://doi.org/10.1093/eurheartj/ehu284
Weissler-Snir A, Allan K, Cunningham K Hypertrophic cardiomyopathy-related sudden cardiac death in young people in Ontario. Circulation. 2019; 140:1706-1716 https://doi.org/10.1161/CIRCULATIONAHA.119.040271
O'Mahony C, Elliott P, McKenna W. Sudden cardiac death in hypertrophic cardiomyopathy. Circ Arrhythm Electrophysiol. 2013; 6:443-451 https://doi.org/10.1161/CIRCEP.111.962043
Sears SF, Shea JB, Conti JB. Cardiology patient page. How to respond to an implantable cardioverter-defibrillator shock. Circulation. 2005; 111:e380-382 https://doi.org/10.1161/CIRCULATIONAHA.104.508663
Elayi CS, Lusher S, Meeks Nyquist JL Interference between dental electrical devices and pacemakers or defibrillators: results from a prospective clinical study. J Am Dent Assoc. 2015; 146:121-128 https://doi.org/10.1016/j.adaj.2014.11.016
Ejection Fraction Heart Failure Measurement. http://www.heart.org (accessed October 2022)
Scottish Dental Clinical Effectiveness Programme. Antibiotic prophylaxis against infective endocarditis implementation advice 2018. http://www.sdcep.org.uk/media/qvpj2kfb/sdcep-antibiotic-prophylaxis-implementation-advice.pdf (accessed October 2022)
NICE. Prophylaxis against infective endocarditis: antimicrobial prophylaxis against infective endocarditis in adults and children undergoing interventional procedures. Clinical Guideline CG64. 2016. http://www.nice.org.uk/guidance/cg64 (accessed October 2022)
Jastak JT, Yagiela JA. Vasoconstrictors and local anesthesia: a review and rationale for use. J Am Dent Assoc. 1983; 107:(4)623-30 https://doi.org/10.14219/jada.archive.1983.0307
Akutsu A, Chiba T, Takahashi H Management of dental problems in patients with cardiovascular disease. J Am Dent Assoc. 1964; 68:333-342 https://doi.org/10.14219/jada.archive.1964.0104
Monheim LM. Local anaesthesia and Pain Control in Dental Practice, 4th edn. St Louis, MO, USA: CV Mosby; 1969
Oosterink FM, de Jongh A, Hoogstraten J. Prevalence of dental fear and phobia relative to other fear and phobia subtypes. Eur J Oral Sci. 2009; 117:(2)135-43 https://doi.org/10.1111/j.1600-0722.2008.00602.x
Craig DC, Boyle CA. Practical Conscious Sedation, 2nd edn. London: Quintessence; 2017
Hohner P, Reiz S. Nitrous oxide and the cardiovascular system. Acta Anaesthesiol Scand. 1994; 38:763-786 https://doi.org/10.1111/j.1399-6576.1994.tb03999.x
Eisele JH, Reitan JA, Massumi RA Myocardial performance and N2O analgesia in coronary-artery disease. Anesthesiology. 1976; 44:16-20 https://doi.org/10.1097/00000542-197601000-00003
Kawamura R, Stanley TH, English JB Cardiovascular responses to nitrous oxide exposure for two hours in man. Anesth Analg. 1980; 59:93-99
Tanaka M, Nishikawa T. Effects of nitrous oxide on baroreflex gain and heart rate variability. Acta Anaesthesiol Scand. 2004; 48:1163-1167 https://doi.org/10.1111/j.1399-6576.2004.00493.x
Scottish Dental Clinical Effectiveness Programme. Management of dental patients taking anticoagulant or antiplatelet drugs. 2022. http://www.sdcep.org.uk/media/ypnl2cpz/sdcep-management-of-dental-patients-taking-anticoagulants-or-antiplatelet-drugs-2nd-edition.pdf (accessed October 2022)
Gibson RM, Meechan JG. The effects of antihypertensive medication on dental treatment. Dent Update. 2007; 34:70-78 https://doi.org/10.12968/denu.2007.34.2.70

Cardiomyopathy and Dentistry

From Volume 49, Issue 10, November 2022 | Pages 795-802

Authors

Shazia Kaka

BDS, MJDF, RCSEng, MSc M Spec Care Dent, BDS MJDF RCS (Ed), MSc, MSCD RCS(Ed), FHEA

Specialty Registrar (STR) in Sedation and Special Care Dentistry, Oxfordshire Healthcare Foundation Trust, UK (shazia.kaka@kcl.ac.uk)

Articles by Shazia Kaka

Email Shazia Kaka

Sarah Couzens

BDS, MFDS, PgCert DE, MSc M Spec Care Dent

Specialist in Special Care Dentistry; Department of Sedation and Special Care Dentistry, Guys and St Thomas NHS Foundation Trust, London

Articles by Sarah Couzens

Carole Ann Boyle

BDS, MMEDSci, MSND, RCSEd, FDS RCSEng, FDS RCSEd, FFDT, FDSRCSEd

Consultant in Special Care Dentistry; Department of Sedation and Special Care Dentistry, Guys and St Thomas NHS Foundation Trust, London

Articles by Carole Ann Boyle

Email Carole Ann Boyle

Abstract

This article considers the clinical implications of cardiomyopathy and how it impacts on the provision of oral care. Consideration is given to the management of pain and anxiety in this patient group and the provision of safe, effective care.

CPD/Clinical Relevance: With an increasingly ageing population, dentists should have the knowledge to safely assess and treat medically compromised patients.

Article

The cardiomyopathies are a diverse group of conditions that affect the shape, structure, and/or thickness of the heart muscle (the myocardium).1 They may affect anyone, at any age, with a current UK prevalence of approximately 1 in 500 people.2 The cause can be primary, with a genetic aetiology, or secondary to autoimmune, inflammatory, endocrine, neurological or infiltrative conditions.1,3 The prevalence of cardiomyopathy is rising, and those who are diagnosed are surviving longer. They are therefore more likely to present to the dental team.

Dental practitioners should have a basic awareness of the condition and know what questions to ask before treating or referring these patients onwards. Careful assessment is required to plan the use of local anaesthesia and sedation techniques.

Types of cardiomyopathy

There are five main types of cardiomyopathy and each affects the myocardium differently.

Dilated cardiomyopathy (DCM)

The chamber of the left ventricle becomes enlarged (dilated), resulting in stretching and thinning of the myocardium. This weakens the ventricle's ability to effectively pump blood into the systemic circulation, thereby reducing systemic perfusion. The heart gradually changes to a more rounded shape, with potential disruption to electrical activity through the heart.1,4 It can be associated with pregnancy, although 70% of women recover within 1-year of diagnosis.4

Hypertrophic cardiomyopathy (HCM)

The muscular walls of the ventricles thicken, thereby reducing the size of its chambers. This thickening stiffens the heart muscle, making it harder for the ventricles to relax and fill with blood, and contract to pump blood out. Left ventricular outflow tract obstruction (LVOTO) is a recognized feature of HCM, where there is an obstruction to forward flow. This results in an increased afterload, which can lead to hypertrophy, dilation and eventual failure of the left ventricle. The degree and location of the thickening will determine symptoms and treatment.1,5

Restrictive cardiomyopathy (RCM)

RCM is less common. Muscular cells (myocytes) become progressively replaced with connective tissue, increasing myocardial stiffness. This predominantly affects the ventricles' ability to relax and fill with blood. As filling decreases, less blood is pumped out into the pulmonary and systemic circulation. The remaining blood ‘backs up’ within the atria, increasing atrial pressure and causing them to enlarge.6

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

ARVC is a rare, more recently described condition. The proteins that hold myocytes together become defective, resulting in the death of myocytes and their replacement with fatty or fibrofatty tissue. This causes myocardial thinning and ventricular dilation. While the condition predominantly affects the right ventricle, it can also affect the left.1

Takutsobo cardiomyopathy (TCM)

TCM is also known as stress-induced cardiomyopathy. It is a fully reversible condition where the left ventricle balloons and weakens, causing acute deterioration of left ventricular function.1,7 It mainly occurs in women following significant emotional or physical stress, such as a bereavement or physical illness.7 While the underlying mechanism is not fully understood, excessive catecholamines are thought to be responsible. Recovery usually occurs within a few weeks; however, delayed recovery (>2 months) has been reported.8

Signs, symptoms and complications of cardiomyopathy

Signs and symptoms depend upon the type and severity of cardiomyopathy. While some individuals may be asymptomatic, and even remain undiagnosed for life, others may develop serious symptoms at a young age, with the need for life-saving treatment.

In general, symptoms develop over time due to the decreased ability of the heart to contract and relax normally, combined with changes in the shape and structure of the myocardium, which disrupts the normal transmission of electrical signals. These changes can result in the following main complications.

Heart failure

Heart failure is a complex syndrome resulting from any functional or structural cardiac disorder that impairs the ability of the heart to function as a pump and support a physiological circulation.9 Heart failure can affect the left side, right side or both sides. In left-sided heart failure, the pumping capacity of the left ventricle is reduced. This results in less blood being delivered to the systemic circulation and more blood backing up via the pulmonary veins, into the lungs. In right-sided heart failure, the decreased pumping ability of the right ventricle results in blood backing up into the peripheral tissues and liver. Resulting signs and symptoms include breathlessness (especially when lying down), fatigue, dizziness/syncope, chest pain, cough and oedema around the abdomen and ankles.9

Arrhythmias

Arrhythmias, which may develop secondary to cardiomyopathy, include:

  • Atrial fibrillation: a tachyarrhythmia caused by erroneous electrical impulses within the atria, causing it to beat in a rapid and uncoordinated way. Atrial fibrillation associated with a fast ventricular rate will lead to less time for ventricular filling. The atrial blood flow becomes ‘turbulent’, reducing pumping efficiency, increasing blood stagnation, and increasing the risk of clot formation and stroke.
  • Ventricular tachycardia: a tachyarrhythmia caused by erroneous electrical activity in the ventricles. This results in rapid ventricular contraction (>100bpm), reduced pumping efficiency and is a primary cause of cardiac arrest.
  • Ventricular fibrillation: uncoordinated contraction of the ventricles and a primary cause of cardiac arrest.

Heart block

Electrical conduction within the heart is blocked or slowed, leading to bradycardia, flow problems and an increased risk of other arrhythmias.

Sudden cardiac death (SCD)

This is a rare complication, occurring due to the sudden development of life-threatening arrhythmias. SCD mainly affects adults in their mid-30s to 40s, and men twice as often as women. While it may be a risk with all cardiomyopathies, HCM is believed to be one of the leading causes, with a variable incidence of 0.84–1% annually.10 While previously thought to be associated with intense physical activity,10 more recent evidence suggests a greater incidence at rest.11

Risk factors for SCD related to hypertrophic cardiomyopathy include:12

  • A family history of sudden cardiac arrest;
  • A history of syncope (fainting episodes of unknown cause);
  • Evidence of severe left ventricular hypertrophy and an increase in left atrial size (from imaging);
  • Heart failure (6–9 times more likely to experience ventricular arrhythmias);
  • Significant changes in blood levels of potassium and magnesium;
  • Obesity;
  • Diabetes;
  • Recreational drug abuse.

Management of cardiomyopathy

Cardiomyopathy cannot be cured, and treatment options aim to help control symptoms.

Pharmacological therapies

The most commonly used drugs, their potential oral manifestations and considerations when delivering oral healthcare are listed in Table 1.


Table 1. Pharmacological drug therapies commonly used in the treatment of cardiomyopathy, and their associated oral considerations.28
Drug type Drug examples Drug mode of action When is it used Oral manifestations Considerations when providing oral healthcare
Beta blockers Bisoprolol, metoprolol, carvedilol Competitive antagonists that block adrenaline and noradrenaline receptor sites, thus reducing myocardial contractility, HR and BP Usually used in combination with an ACE inhibitor or angiotensin II receptor blocker as a standard treatment for heart failure. Also used in hypertrophic obstructive cardiomyopathy Dry mouthLichenoid reactionsNumbness of peri-oral structuresTaste changes NSAIDs can decrease hypotensive effect IV sedation with midazolam can increase hypotensive effect
ACE inhibitors Perindopril, ramipril, captopril, lisinopril Block the conversion of angiotensin I to II by inhibiting ACE in the renin–angiotensin system – leads to vasodilation and a drop in BP Usually prescribed in combination with a beta blocker or angiotensin II receptor blocker as a standard treatment for heart failure Angiodema (1%)Dry mouthLichenoid reactionsGlossitisErythema multiformeBurning mouthLoss of tasteTaste changes IV sedation with midazolam can increase hypotensive effect
Angiotensin receptor blockers Valsartan, losartan, candesartan Selectively inhibit angiotensin II via competitive inhibition of the angiotensin II receptor Usually prescribed in combination with a beta blocker or ACE inhibitor as a standard treatment for heart failure Dry mouth Angiodema Taste loss Cough IV sedation with midazolam can increase hypotensive effect
Potassium-sparing diuretics Spironolactone Decrease sodium reabsorption within the kidneys. As more sodium is lost in the urine, increased diuresis occurs with a subsequent drop in BP Usually prescribed, in conjunction with standard treatment for heart failure, when symptoms of heart failure persist Steven–Johnson syndromeLichenoid reactionsDry mouth and altered taste IV sedation with midazolam can increase hypotensive effect
Selective If current inhibitor Ivabradine Partially blocks the current generated by the sino-atrial node, thereby reducing HR Additional treatment option when standard heart failure treatments or second line treatments are not fully effective    
Positive inotropes Milrinone (given IV) Increases cardiac contractility, cardiac relaxation and vasodilatation, thereby increasing cardiac output Short-term treatment of acute heart failure or severe congestive heart failure that is unresponsive to conventional therapy. Not indicated for heart failure secondary to HCM   Patient should receive dental care in secondary care
Calcium channel blockers Verapamil Inhibits the influx of calcium into myocardial cells, thereby preventing depolarization, and reducing myocardial contractility and HR Commonly used for hypertrophic obstructive cardiomyopathy. Relaxation of the heart results in a reduction in the level of obstruction, thereby improving symptoms Drug-induced gingival enlargement IV sedation with midazolam can increase hypotensive effect
Anticoagulants DOACs (eg apixaban, rivaroxaban, dabigatran, edoxaban) Inhibit specific coagulation factors, thus reducing the risk of clot formation Commonly used in patients with atrial fibrillation to reduce the risk of clot formation and subsequent stroke   Increased bleeding risk when carrying out invasive procedures. Dental care should be planned in accordance with SDCEP anticoagulation guidance23
Warfarin Antagonizes vitamin K which is responsible for the production of coagulation factors II, VII, IX, X

ACE: angiotensin-converting enzyme; BP: blood pressure; HCM: hypertrophic cardiomyopathy;HR: heart rate; IV: intravenous; NSAID: non-steroidal anti-inflammatory.

Implantable cardioverter defibrillator (ICD)

ICDs are placed in those at high risk of developing dangerous arrhythmias. On detecting an abnormal rhythm, the ICD delivers either small rapid pacing impulses, or a larger electric shock, to restore normal rhythm. Patients who experience a shock will often feel startled and may be distressed.

In the case of a shock being experienced within a dental setting, the dental team should reassure the patient and stop dental care.13 If they recover quickly, the patient should be encouraged to contact their cardiologist. In the case of ongoing chest pain, shortness of breath, dizziness or confusion, emergency medical help should be sought immediately.

Permanent pacemaker (PPM)

Patients with heart block or bradyarrhythmias may benefit from the placement of a permanent pacemaker. This helps augment and regulate electrical impulses already produced by their heart, thus ensuring an adequate, regular rate. Although there is some concern about using ultrasonic devices on these patients, a small prospective study found no interference between dental electrical devices and pacemakers.14

Heart transplant

This is the last resort for heart failure. Before a patient is added to the transplantation list, a dental assessment should be carried out. Teeth with the potential to become acutely infected in the post-transplant period should be treated, as long as the urgency of the transplant does not preclude it. The ASA status of the patient should be considered, with most patients requiring treatment in a hospital setting.

If a patient is ineligible for transplantation or needs support while waiting for a heart, a left ventricular assist device (LVAD) can help improve survival and quality of life. Patients with these devices should be treated in a hospital environment with cardiac monitoring and medical support available.

Managing dental patients with cardiomyopathy

History taking

Questioning will ascertain the severity of the cardiomyopathy, the presence and severity of any complications, and any special considerations needed when providing care (Table 2). If patients are unable to answer these questions, or there is any doubt as to the information provided, correspondence with the GMP or cardiology teams is advised.


Table 2. Questions to be asked when taking a medical history from a patient with cardiomyopathy.
What type of cardiomyopathy do you have? As the pathogenesis of all cardiomyopathies is different, this may affect the most appropriate pain and anxiety management option
Who manages your cardiomyopathy and how often are you reviewed? A patient who is regularly reviewed by a cardiologist in secondary care is more likely to have severe disease or an increased risk of complications than an individual who is infrequently followed up by their general medical practitioner
Are you on any medication? Patients on a greater number of pharmacological therapies are more likely to have more severe disease and a greater risk of complications
Do you have an implanted heart device? If an ICD is in place, how regularly do you experience shocks? When was the last time you had a shock? Patients with an ICD are at high risk of developing dangerous arrhythmias, with the frequency of shocks indicating how regularly and how recently this has occurredIf a patient has a left ventricular assist device, their heart failure is severe, and they can be considered ASA 4
Is treatment of your cardiomyopathy planned? What will this be? This gives an indication of how stable their condition is. If future treatment is required, it suggests worsening disease. The type of planned treatment will help determine the complications they may have/are at risk of
Do you get breathless/tired/dizzy? Patients may indicate they get more breathless/have an increased cough when lying down if they have heart failure. Other indicators of heart failure include general fatigue and regular dizziness/syncope
Do you have a family history of cardiomyopathy? Have any family members had significant problems with it? Patients may disclose sudden cardiac death among family members, in which case they will also be at increased risk

For symptomatic patients under the care of a cardiologist, the following questions should be asked:

What is the ejection fraction (EF)?

This is a measurement, expressed as a percentage, of the total volume of blood ejected from the left ventricle during contraction, when compared to the total volume of blood present within the left ventricle. It correlates strongly with left ventricular function, with the EF of a healthy heart usually between 50% and 60%. In someone with cardiomyopathy, the EF will usually be under 45%. Heart failure is considered to occur below an EF of 40%, but can also occur with a normal EF.15 DCM and HCM can present with different ejection fractions, but have similar symptoms.

HCM in particular may initially present with a higher ejection fraction as the heart attempts to ‘compensate.’ This cannot be sustained and will eventually reduce.15

Is antibiotic cover required for invasive dental procedures?

Patients with hypertrophic cardiomyopathy are deemed to be at increased risk of infective endocarditis.16,17 While they are not in the special consideration group for antibiotic prophylaxis, it should nonetheless be considered in liaison with the cardiology team. SDCEP guidance outlines the appropriate discussions that should be held with the patient, including advice on prescribing and administration of antibiotic prophylaxis.16 Invasive dental procedures are listed in Table 3.


Table 3. Invasive dental procedures.
Invasive dental procedures Non-invasive dental procedures
Placement of matrix bands Infiltration or block local anaesthetic injections in non-infected soft tissues
Placement of subgingival rubber dam clamps BPE screening
Sub-gingival restorations including fixed prosthodontics Supra-gingival scale and polish
Endodontic treatment before apical stop is established Supra-gingival restorations
Pre-formed metal crowns Supra-gingival orthodontic bands and separators
Full periodontal examination (including pocket charting in diseased tissues) Removal of sutures
Root surface instrumentation/subgingival scaling Radiographs
Incision and drainage of abscess Placement or adjustment of orthodontic or removable prosthodontic appliances
Dental extractions
Surgery involving elevation of a muco-periosteal flap or muco-gingival area
Placement of dental implants
Uncovering implant sub-structures
(reproduced from SCDEP guidance16)

Examination

Patients who report breathlessness/dizziness/tiredness should be examined further for signs of heart failure. The patient may struggle to lie back in the chair due to difficulty breathing (orthopnea). They may present with a cough or signs of fluid retention around their ankles or abdomen. Oxygen saturations may be reduced, and heart rate increased. It is important that dentists consider patient positioning. They may ask how the patients sleeps at night, or the number of pillows required. In most cases, it will be important not to lie the patient completely flat as this will worsen the patient's orthopnoea.

Generally, the greater the severity of a patient's symptoms, the more severe their disease is likely to be. For example, individuals who can climb stairs with only mild breathlessness will have less severe disease than an individual who is breathless at rest. Table 4 describes the New York Heart Association Classification for Heart Failure. As part of an overall dental assessment, it is worth considering which stage applies to the patient. This will help dictate their overall ASA status and the likely safety of pain/anxiety management options.


Table 4. New York Heart Association Classification for Chronic Heart Failure.
Class 1 No limitations Ordinary physical activity does not cause undue fatigue, dyspnoea or palpitations
Class II Slight limitation of physical activity Ordinary physical activity results in fatigue, palpitation, dyspnoea or angina
Class III Marked limitation of physical activity Less than ordinary physical activity leads to symptoms
Class IV Unable to carry on any physical activity without discomfort Symptoms of heart failure present at rest

Pain and anxiety management options for patients with cardiomyopathy

Local anaesthesia (LA): the use of vasoconstrictors

The use of local anaesthetic (LA) with adrenaline for patients with cardiovascular compromise has been debated for decades.18

Adrenaline is a catecholamine that acts on alpha and beta adrenoreceptors in the sympathetic nervous system. It increases blood pressure (BP), myocardial contractility and heart rate (HR) via a dose-dependent relationship. For patients with pre-existing heart failure or a compromised cardiac status, even a small amount of systemically absorbed adrenaline may precipitate these changes and increase the risk of a tachyarrhythmia.

Excluding adrenaline, however, also has disadvantages. As it is a vasoconstrictor, it improves haemostasis at the treatment site, while also delaying systemic absorption of the LA agent, thereby reducing LA toxicity risk, and enhancing the intensity and duration of the LA effect. Adequate LA is particularly important for patients with cardiovascular compromise as pain, stress and anxiety can release high quantities of endogenous adrenaline and noradrenaline, arguably more capable of leading to adverse cardiac events.

The American Heart Association (AHA) and American Dental Association (ADA) advise that a vasoconstrictor is appropriate as long as preliminary aspiration is used, the agent is injected slowly, and the lowest effective dose is administered.19 It has also been suggested that, while the maximum dose of adrenaline for a healthy subject is 0.2 mg, the dose for patients with more severe CV disease (ASA III and IV) should not exceed 0.04 mg.20

The most commonly used dental anaesthetics in the UK are 2% lidocaine with 1:80,000 adrenaline, 4% articaine with 1:200,000 adrenaline and 4% articaine with 1:100,000 adrenaline. Table 5 shows the amount of adrenaline in each dental cartridge and the safe limits when following ADA advice.


Table 5. Local anaesthetic limits for ASA III/IV cardiovascularly compromised patients under ADA/AHA advice.20
Standard dental cartridge Adrenaline present within dental cartridge Safe limit according to ADA advice
2.2 ml 2% lidocaine with 1:80,000 adrenaline 1:80000 adrenaline = 1 g adrenaline in 80,000 ml = 1 mg adrenaline in 80 ml = 0.0275 mg adrenaline in 2.2 ml 1.5 cartridges
2.2 ml 4% articaine with 1:100,000 adrenaline 1:100,000 adrenaline = 1 g adrenaline in 100000 ml = 1 mg adrenaline in 100 ml = 0.022 mg adrenaline in 2.2 ml 2 cartridges
2.2 ml 4% articaine with 1:200,000 adrenaline 1:200,000 adrenaline = 1 g adrenaline in 200,000 ml = 1 mg adrenaline in 200 ml= 0.011 mg adrenaline in 2.2 ml 4 cartridges

Felypressin (Octapressin), a synthetic analogue of vasopressin, is an alternative to adrenaline in helping promote local haemostasis. At lower concentrations, it produces no significant alterations to HR, BP or myocardial contractility. In the UK, it is supplied with 3% prilocaine (Citanest) in a 2.2-ml cartridge. It is therefore suggested that for patients with HCM and TCM, prilocaine with felypressin should be used as the LA of choice, whereas for patients with DCM, RCM and ARVC, it can be considered as an adjunct if further LA is required after reaching the safe ADA limit (Table 3). Plain LA may also be used; however, this should be weighed up with ensuring adequate pain, anxiety and bleeding control.

Conscious sedation

In total, 13–20% of adults are dentally anxious, with an additional 4% having a dental phobia.21 While dental treatment will provoke a stress reaction to some extent in all patients, those with heightened anxieties or phobias may hypersecrete endogenous catecholamines. This may significantly increase the risk of arrhythmias or an acute event such as TCM. Additional anxiety management options may therefore be recommended for these patients.

Inhalation nitrous oxide–oxygen sedation

Inhalation sedation is a non-invasive, conscious sedation technique that uses a combination of nitrous oxide and oxygen to produce anxiolysis, mood alteration, muscle relaxation and analgesia.22 It is a useful adjunct for patients with a mild to moderate anxiety to dentistry. It is delivered via a nasal hood (mask), with the ratio of nitrous oxide to oxygen being gradually increased till the patient feels sufficiently anxiolysed. The maximum concentration of nitrous oxide that can be given is 70%.22

The effects of nitrous oxide on the cardiovascular system have been debated. Some suggest that nitrous oxide has no effects on heart rate, rhythm or output,23 while others advise that there is a weak direct myocardial depressant action, especially in patients with left ventricular hypofunction, or when the titrated concentration is increased beyond 40%.24,25

Intravenous sedation (IVS)

IVS with midazolam is the most used conscious sedation technique in dentistry, producing anxiolysis, muscle relaxation, hypnosis and amnesia.21 It is a useful adjunct to enable comfortable, stress-free dentistry in patients who have a moderate to severe dental anxiety. Midazolam is a benzodiazepine that produces cardiovascular effects, including a decrease in mean arterial pressure, cardiac output, stroke volume and systemic vascular resistance.21 Usually, these changes are compensated by the baroreceptor reflex, which works to increase blood pressure, thereby making these effects negligible. However, in patients with cardiomyopathy, these changes may be enhanced, resulting in reduced systemic perfusion. When coupled with respiratory depression, adverse cardiac events may occur.

General anaesthesia (GA)

Many of the drugs commonly used in GA may affect the cardiovascular system. For an individual with more severe disease, it is not the first choice for pain and anxiety management. It may be required occasionally, for example, if the patient is severely anxious and requires invasive, multiquadrant dentistry. Patients with less severe disease may be suitable for a day-case procedure following a pre-operative assessment, while those with more severe complications will require an inpatient admission.

Bleeding risk

An isolated cardiomyopathy is rarely a cause for bleeding in itself. However, it is important to consider complications of the condition. One sequelae of heart failure may be hepatic dysfunction with a resultant reduction in clotting factors. In patients with a reduced ejection fraction, blood may pool in the left ventricle, increasing the chance of intraventricular thrombosis. In others, there may be a high risk of atrial fibrillation. These conditions are commonly treated with antiplatelet medication (clopidogrel) or anticoagulants (warfarin or apixaban). For those on heparin requiring invasive dental procedures, correspondence with the cardiologist would be required. Usually, omission of the anticoagulant on the day of the procedure is adequate. Guidance for other anticoagulant or antiplatelet medications can be found in the SDCEP guidelines.27 Local haemostatic management should be used post-operatively.

Location of treatment

The decision of whether to treat patients in primary or secondary care depends on a number of factors:

  • Their cardiac risk;
  • Their other medical comorbidities and overall ASA status;
  • Their dental anxiety;
  • Their treatment needs, with consideration towards the complexity and duration of the procedure;
  • The confidence/experience of the practitioner in managing medically complex patients and medical emergencies if one was to arise.

Symptomatic cardiac patients, or those with severe disease, who have moderate to severe anxiety are best treated in a secondary care environment where appropriate monitoring and medical support can be arranged. This is especially so if requiring more complex dental treatment or treatment that is likely to take a longer time. Alternatively, asymptomatic or stable patients with no other relevant medical history, minimal anxiety or requiring simple/short treatments are best suited to primary care. Ultimately, this is a case-by-case decision.

Conclusion

People with cardiomyopathy are a complex group and require a thorough risk assessment prior to the provision of dental care. While many cases can be safely provided by the GDP with additional knowledge, the provision of sedation and general anaesthesia are better provided in a secondary care environment.